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Endothelial Cells: From Mechanisms of Dysfunction to Therapeutic Targets
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Endothelial Cells: From Mechanisms of Dysfunction to Therapeutic Targets

A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Endocrinology & Metabolism".

Deadline for manuscript submissions: closed (25 February 2022) | Viewed by 7345

Special Issue Editor

Dr. Nadia Jahroudi

E-Mail Website1 Website2
Guest Editor
Department of Medicine, University of Alberta, Edmonton, AB T6G 2S2, Canada
Interests: von Willebrand factor; endothelial cells; transcription; gene regulation

Special Issue Information

Dear Colleagues,

Over the past 70 years, our understanding of the role of the endothelial cells that line all of our blood vessels has advanced from them being viewed as an inert barrier to now being understood as a complex secretory and sensory organ, which is the first responder to blood borne physiological and pathophysiological components. The endothelium plays key roles in blood vessel formation, regulation of blood flow and thus tissue perfusion, hemostasis, inflammation. Endothelial dysfunction, and altered response to stimuli, can occur as a result of aging and/or in chronic conditions such as diabetes and obesity. This is associated with increased risk of cardiovascular disease and its clinical consequences such as heart attack, stroke and peripheral vascular disease. Understanding of the molecular mechanisms underlying endothelial dysfunction is essential for development of effective and targeted therapeutic interventions.

In this Special Issue, we will provide a review of recent advances in our understanding of the mechanisms underlying endothelial dysfunction in relation to risk factors such as metabolic derangement and aging; and explore new areas such as the potential role of perivascular adipose tissue and the gut microbiome in development of vascular disease.

Dr. Nadia Jahroudi
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Journal of Clinical Medicine is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Endothelial cells
  • Endothelial dysfunction
  • Hemostasis
  • Aging
  • Diabetes
  • Obesity
  • Hypoxia
  • Cardiovascular disease

Published Papers (3 papers)

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Research

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8 pages, 1539 KiB  
Article
Prohibitin 1 Regulates Inflammatory Mediators and Reactive Oxygen Species in Retinal Endothelial Cells
by Li Liu, Youde Jiang and Jena J. Steinle
J. Clin. Med. 2022, 11(7), 1915; https://doi.org/10.3390/jcm11071915 - 30 Mar 2022
Cited by 2 | Viewed by 1587
Abstract
Diabetic retinopathy is associated with increased inflammatory mediator levels. In these studies, we focused on prohibitin 1. We performed western blotting for retinal lysates from diabetic mice and Epac1 floxed and cdh5Cre-Epac1 mice. We also grew primary retinal endothelial cells (REC) in normal [...] Read more.
Diabetic retinopathy is associated with increased inflammatory mediator levels. In these studies, we focused on prohibitin 1. We performed western blotting for retinal lysates from diabetic mice and Epac1 floxed and cdh5Cre-Epac1 mice. We also grew primary retinal endothelial cells (REC) in normal (5 mM) and high (25 mM) glucose, and treated some cells with an Epac 1 agonist or prohibitin 1 siRNA. Western blotting was done to confirm knockdown of prohibitin 1 and Epac 1 agonism. We measured the tumor necrosis factor alpha (TNFα), interleukin-1-beta (IL-1β), phosphorylated prohibitin 1, phosphorylated nuclear factor kappa beta (NFkB), high mobility group box 1 (HMGB1) and reactive oxygen species (ROS) levels in REC after transfection with prohibitin 1 siRNA. Results showed that high glucose increased the inflammatory mediators, as well as HMGB1 and ROS. The levels of ROS, HMGB1, and inflammatory pathways were all reduced after cells were transfected with prohibitin 1 siRNA. Epac1 reduced prohibitin 1 phosphorylation. In conclusion, decreased prohibitin 1 significantly reduced the inflammatory mediator and ROS levels in REC. Epac1 regulates the prohibitin 1 levels in REC. Full article
(This article belongs to the Special Issue Endothelial Cells: From Mechanisms of Dysfunction to Therapeutic Targets)
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Review

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14 pages, 317 KiB  
Review
The Effect of Hyperlipidemia on the Course of Diabetic Retinopathy—Literature Review
by Anna Bryl, Małgorzata Mrugacz, Mariusz Falkowski and Katarzyna Zorena
J. Clin. Med. 2022, 11(10), 2761; https://doi.org/10.3390/jcm11102761 - 13 May 2022
Cited by 9 | Viewed by 2395
Abstract
Diabetes mellitus is a very important social issue, and its retinal complications continue to be one of the major causes of blindness worldwide. The effect of glucose level on the development of retinal retinopathy has been the subject of numerous studies and is [...] Read more.
Diabetes mellitus is a very important social issue, and its retinal complications continue to be one of the major causes of blindness worldwide. The effect of glucose level on the development of retinal retinopathy has been the subject of numerous studies and is well understood. Hypertension and hyperlipidemia have been known to be important risk factors in the development of diabetes complications. However, the mechanisms of this effect have not been fully explained and raise a good deal of controversy. The latest research results suggest that some lipoproteins are closely correlated with the incidence of diabetic retinopathy and that by exerting an impact on their level the disease course can be modulated. Moreover, pharmacotherapy which reduces the level of lipids, particularly by means of statins and fibrate, has been shown to alleviate diabetic retinopathy. Therefore, we have decided to review the latest literature on diabetic retinopathy with respect to the impact of hyperlipidemia and possible preventive measures Full article
(This article belongs to the Special Issue Endothelial Cells: From Mechanisms of Dysfunction to Therapeutic Targets)
21 pages, 1119 KiB  
Review
Age-Associated Increase in Thrombogenicity and Its Correlation with von Willebrand Factor
by Parnian Alavi, Abhisha M. Rathod and Nadia Jahroudi
J. Clin. Med. 2021, 10(18), 4190; https://doi.org/10.3390/jcm10184190 - 16 Sep 2021
Cited by 12 | Viewed by 2703
Abstract
Endothelial cells that cover the lumen of all blood vessels have the inherent capacity to express both pro and anticoagulant molecules. However, under normal physiological condition, they generally function to maintain a non-thrombogenic surface for unobstructed blood flow. In response to injury, certain [...] Read more.
Endothelial cells that cover the lumen of all blood vessels have the inherent capacity to express both pro and anticoagulant molecules. However, under normal physiological condition, they generally function to maintain a non-thrombogenic surface for unobstructed blood flow. In response to injury, certain stimuli, or as a result of dysfunction, endothelial cells release a highly adhesive procoagulant protein, von Willebrand factor (VWF), which plays a central role in formation of platelet aggregates and thrombus generation. Since VWF expression is highly restricted to endothelial cells, regulation of its levels is among the most important functions of endothelial cells for maintaining hemostasis. However, with aging, there is a significant increase in VWF levels, which is concomitant with a significant rise in thrombotic events. It is not yet clear why and how aging results in increased VWF levels. In this review, we have aimed to discuss the age-related increase in VWF, its potential mechanisms, and associated coagulopathies as probable consequences. Full article
(This article belongs to the Special Issue Endothelial Cells: From Mechanisms of Dysfunction to Therapeutic Targets)
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